The proposed studies are designed to study the "tension-reduction hypothesis" for alcohol consumption by using animal models to examine the effects of stress and ethanol on brain neurochemistry. The animal models used will be the long-sleep (LS) and short-sleep (SS) mice which differ in CNS sensitivity to ethanol, recombinant inbreds of LS and SS mice, and various inbred strains of mice. Ethanol in humans and in animals produces a release of adrenal steroid hormones. It is known that ethanol differentially induces corticosterone release in various genetic stocks of mice, but the consequences of this release are unknown. Furthermore, it has been proposed that steroid hormones can modify GABAergic function in the CNS. We propose to examine the hypothesis that some of ethanol's acute actions are mediated via activation of corticosterone release either directly, or indirectly by an interaction with the GABAergic system. Ethanol's acute low-dose anxiolytic actions and high-dose sedative actions will be examined before and after mild stress. These studies will measure brain glucocorticoid receptors and GABAergic receptors. Animals will be adrenalectomized and steroid replacement studies will be performed to examine the role of corticosterone in CNS response to ethanol. Genetic correlational studies will be performed to examine the relationship between corticosterone release and behavioral actions of ethanol.